Falso incremento de la hormona estimulante del tiroides asociado a la presencia de macro-TSH / Falsely elevated levels of thyrotropin caused by macro-TSH

Mujer que presentó un importante incremento de la hormona estimulante del tiroides (TSH) (62,2 mU/L) con hormonas tiroideas dentro de los intervalos de referencia. La paciente se encontraba eutiroidea y no presentaba bocio. Se realizó un estudio inicial para determinar la posible causa del incremento en la concentración de TSH. La recuperación de TSH tras precipitación con polietilenglicol fue del 1%, sugiriendo la presencia de alguna molécula de elevado peso molecular que podría interferir en la determinación. Mediante cromatografía de exclusión, se confirmó la presencia de macro-TSH, un complejo autoinmune formado por TSH unido a una Inmunoglobulina G que es inmunorreactivo pero biológicamente inactivo, por lo que, si no se detecta, induce a una interpretación errónea de la concentración de TSH (AU)

Woman showing an important increase of serum TSH (62.2 mU/L) with thyroid hormones within the reference interval. The patient was clinically euthyroid and without goitre. Investigations were carried out to determine the origin of the unexpected high TSH. Polyethylene glycol precipitation test showed low TSH recovery (1%), indicating the presence of large molecules that could interfere with the measurement. The serum sample was fractionated by gel filtration chromatography and the presence of a macro-TSH form was confirmed, an immunoreactive but biologically inactive TSH-Immunoglobulin G autoantibody complex. Its detection is important to avoid a misleading interpretation of the TSH concentration (AU)

Cadmium chronotoxicity at pituitary level: effects on plasma ACTH, GH, and TSH daily pattern

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Cadmium is an endocrine disruptor that has been shown to induce chronotoxic effects. The present study was designed to evaluate the possible cadmium effects on the daily secretory pattern ofadrenocorticotropin hormone (ACTH), growth hormone (GH), and thyroid-stimulating hormone (TSH)in adult male Sprague-Dawley rats. For this purpose, animals were treated with cadmium at two different doses [25 and 50 mg/l cadmium chloride (CdCl2)] in the drinking water for 30 days. Control age-matched rats received cadmium-free water. After the treatment, rats were killed at six different time intervals throughout a 24-h cycle. Cadmium exposure modified the 24-h pattern of plasmaACTH and GH levels, as the peak of ACTH content between 12:00 and 16:00 h in controls appeared at 12:00 h in the group treated with the lowest dose used, while it appeared between 16:00 and 20:00 h in rats exposed to 50 mg/l CdCl2. In addition, the peak of GH content found at 04:00 h in controls moved to 16:00 h in rats exposed to 25 mg/l CdCl2, and the highest dose used abolished 24-h changes of GH secretion. The metal treatment did not modify ACTH secretory pattern. Exposure to cadmium also increased ACTH and TSH medium levels around the clock with both doses used. These results suggest that cadmium modifies ACTH and TSH medium levels around the clock, as well as disrupted ACTH and GH secretory pattern, thus confirming the metal chronotoxicity at pituitary level (AU)